Lipopolysaccharide Induces Human Olfactory Ensheathing Glial Apoptosis By Promoting Mitochondrial Dysfunction And Activating The JNK-Bnip3-Baxpathway

Objective:The mechanism of injury and apoptosis of human olfactory ensheathing glia(OEG)in vitro were observed by the inflammatory response model induced by lipopolysaccharide(LPS),so as to clarify the specific pathological molecular process of human olfactory ensheathing glia cell death under inflammatory conditions.It provides a potential therapeutic target for human olfactory ensheathing glia to resist the stress of chronic inflammation.Methods : After the successful induction of inflammatory response model by lipopolysaccharide,the pathological mechanism of OEG death was confirmed by the detection of cell viability,apoptosis,cysteinyl aspartate specific proteinase(Capase)3activity,mitochondrial function,mitochondrial division and mitochondrial apoptosis.The detection of mitochondrial function includes the detection of reactive oxygen species(Ros),antioxidant activity and mitochondrial respiratory enzymes;mitochondrial division includes the detection of mitochondrial division-related proteins and mitochondrial fluorescence;mitochondrial apoptosis includes the detection of mitochondrial apoptotic proteins,mitochondrial apoptotic protein exudation,cysteinyl aspartate specific proteinase(Capase)9 activity.Results :(1)LPS reduces OEG viability in a dose-dependent manner.(2)LPS mediates mitochondrial oxidative stress and energy disorder.(3)LPS triggers mitochondrial fragmentation.(4)LPS activates mitochondrial apoptosis via Bax upregulation and Htr A2/Omi2 release.(5)LPS modulates Bax activation via the JNK-Bnip3 pathway(6)LPS modulates Bax activation via the JNK-Bnip3 pathway.Conclusion : Our study found that LPS-induced inflammation stress reduces OEG viability by mediating mitochondrial injury in a manner dependent on the JNK-Bnip3-Bax pathway.